The aim of this project is to identify the relative role of various lymphocyte populations in disease production in experimental allergic encephalomyelitis, a model of autoimmune disease. These results will focus on the ability to transfer EAE with various populations of lymphocytes, particularly T and B-cell populations. The relationship of the host genetic makeup to disease susceptibility will also be examined, both in vitro and in vivo. The immune response to myelin basic protein is being assessed by measuring antibody and in vitro proliferative responses in various strains of both mice and rats. The chemical components of myelin basic protein are responsible for disease production. T-cell proliferation and reactivity with antibody are being studied. Immune mechanisms in experimental autoimmune myasthenia gravis are also being investigated.